Sotalol for refractory sustained ventricular tachycardia and nonfatal cardiac arrest

The efficacy and safety of sotalol were assessed by electrophysiologic testing and ambulatory recordings in 16 patients with recurrent sustained ventricular tachycardia (VT) or nonfatal cardiac arrest who were refractory to an average of 4.8 conventional antiarrhythmic agents. Twenty-four-hour ambulatory recordings were performed before and after sotalol therapy. Fourteen patients underwent baseline electrophysiologic study and sustained VT was inducible in 12. Oral sotalol (320 to 960 mg/day) completely suppressed inducible sustained VT in 7 patients (58%), with modification in 3 (25%). Ventricular premature complexes were suppressed from baseline (mean +/- standard deviation) 431 +/- 616 to 60 +/- 110/hr (p less than 0.03). After a mean follow-up of 19 +/- 7 months, 12 of 14 patients receiving sotalol treatment had successful suppression of ventricular premature complexes (60 +/- 85/hr) and remained clinically free of sustained VT, except 2 who needed additional antiarrhythmic drugs to suppress the recurrent sustained VT. One patient died suddenly after 25 months of sotalol treatment. No severe side effects were noted during sotalol therapy. This study demonstrates that sotalol is a well-tolerated, effective antiarrhythmic agent in patients at high-risk for sudden death. It appears to be beneficial in patients who did not benefit from multiple drug treatment.     

Survival after cardiac arrest or sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy.

OBJECTIVES: The aim of this study was to evaluate the survival of patients with hypertrophic cardiomyopathy (HCM) after resuscitated ventricular fibrillation or syncopal sustained ventricular tachycardia (VT/VF) when treated with low dose amiodarone or implantable cardioverter defibrillators (ICDs). BACKGROUND: Prospective data on clinical outcome in patients with HCM who survive a cardiac arrest are limited, but studies conducted before the widespread use of amiodarone and/or ICD therapy suggest that over a third die within seven years from sudden cardiac death or progressive heart failure. METHODS: Sixteen HCM patients with a history of VT/VF (nine male, age at VT/VF 19 +/- 8 years [range 10 to 36]) were studied. Syncopal sustained ventricular tachycardia/ventricular fibrillation occurred during or immediately after exertion in eight patients and was the initial presentation in eight. One patient had disabling neurologic deficit after VT/VF. Before VT/VF, two patients had angina, four had syncope and six had a family history of premature sudden cardiac death. After VT/VF all patients were in New York Heart Association class I or II, three had nonsustained VT during ambulatory electrocardiography and 11 had an abnormal exercise blood pressure response. After VT/VF eight patients were treated with low dose amiodarone and six received an ICD. Prophylactic therapy was declined by two patients. RESULTS: Mean follow-up was 6.1 +/- 4.0 years (range 0.5 to 14.5). Cumulative survival (death or ICD discharge) for the entire cohort was 59% at five years (95% confidence interval: 33% to 84%). Thirteen (81%) patients were alive at last follow-up. Two patients died suddenly while taking low dose amiodarone, and one died due to neurologic complications of his initial cardiac arrest. Three patients had one or more appropriate ICD discharges during follow-up; the times to first shock after ICD implantation were 23, 197 and 1,124 days. CONCLUSIONS: This study shows that patients with HCM who survive an episode of VT/VF remain at risk for a recurrent event. Implantable cardioverter defibrillator therapy appears to offer the best potential benefit regarding outcome.     

Sustained ventricular arrhythmias: differences between survivors of cardiac arrest and patients with recurrent sustained ventricular tachycardia

Clinical, angiographic, echocardiographic and electrophysiologic data were examined in 101 patients with a history of sustained ventricular arrhythmia not associated with acute myocardial infarction. These patients included 66 survivors of out of hospital cardiac arrest and 35 patients presenting with hemodynamically well tolerated sustained ventricular tachycardia. On univariate analysis, patients in the cardiac arrest group had a lower incidence of previous myocardial infarction and left ventricular aneurysm and a higher ejection fraction compared with the ventricular tachycardia group. During electrophysiologic testing, the arrhythmia induced in the patients in the cardiac arrest group was fast and polymorphic and frequently degenerated into ventricular fibrillation. In contrast, in the ventricular tachycardia group, a slower, monomorphic and hemodynamically well tolerated ventricular tachycardia was commonly induced. On multivariate analysis, a polymorphic pattern of the induced ventricular arrhythmia was the only independent variable that distinguished the survivors of cardiac arrest from those presenting with sustained ventricular tachycardia. These results suggest that 1) the survivors of cardiac arrest and patients presenting with sustained well tolerated ventricular tachycardia are clinically distinct groups; and 2) the polymorphic tachycardia induced during programmed electrical stimulation in the survivors of cardiac arrest may indicate an unstable tachycardia mechanism. This may explain why these patients present with ventricular fibrillation and cardiac arrest, whereas others present with hemodynamically stable ventricular tachycardia.     

Diagnosis and therapy of ventricular tachycardia in heart failure

In a survey diagnostic and therapeutic problems of the ventricular arrhythmias in cardiac insufficiency are described. It is expressed that prevalence and prognosis of the arrhythmia in cardiac insufficiency are not yet sufficiently investigated both in the acute and in the chronic phase. Furthermore, ascertained investigations concerning the effect of the individual antiarrhythmic drugs have not come to hand. Certain situations and preliminary electrocardiographic findings are to be regarded as premonitory signs; in the individual case they are entitled to a prophylactic therapy with antiarrhythmic drugs. The consideration of pharmacokinetic laws is particularly significant in the disturbed metabolization and the reduction of the hepatic blood in this phase.     

Prognosis of patients with sustained ventricular tachycardia and of survivors of cardiac arrest not inducible by programmed stimulation.

The aim of this study was to analyze the long-term clinical outcome of 60 prospectively studied patients with documented sustained ventricular tachyarrhythmia that was not inducible during baseline programmed ventricular stimulation: 39 with cardiac arrest due to noninfarction ventricular fibrillation (VF) and 21 with mild hemodynamically compromising sustained ventricular tachycardia (VT). Left ventricular ejection fraction was 55 +/- 14% in the VF group and 50 +/- 13% in the VT group (difference not significant). Patients were discharged without conventional antiarrhythmic drugs and received only empirical beta-blocker therapy. During a mean follow-up period of 21 +/- 16 months (mean +/- SD), 10 of 60 patients (17%) died suddenly. The actuarial incidence of sudden death at 1 and 4 years was similar in both groups (VF group, 10 and 20%; VT group, 16 and 16%) (p = 0.48). The actuarial incidence of sudden cardiac death was significantly higher in patients with left ventricular ejection fraction < or = 40% than in those with > 40% (1-year incidence in VF group, 40 vs 0%; VT group, 50 vs 0%) (p = 0.005 and p = 0.01, respectively). Multivariate regression analysis identified left ventricular ejection fraction < or = 40% and previous myocardial infarction as the only independent predictor of sudden cardiac death. The occurrence of frequent ventricular pairs during Holter monitoring was the only independent predictor of sustained VT recurrences. It is concluded that patients with sustained ventricular tachyarrhythmia in whom arrhythmia was non-inducible during baseline ventricular stimulation and not treated with antiarrhythmic therapy have a favorable outcome if left ventricular ejection fraction is high.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antiarrhythmic drug therapy for sustained ventricular tachycardia

VT may be observed to accompany a wide variety of heart diseases and occasionally no heart disease at all. The efficacy of drug therapy is dependent on antiarrhythmic effects and the mechanism underlying the patient's VT. Conventional antiarrhythmic agents appear to be effective in no more than one third of patients, but a substantial number of other potentially useful antiarrhythmic agents exist. Unfortunately, their effectiveness in treating sustained VT for the most part must still be proved. Other agents such as amiodarone appear effective, but ways to predict which patients will benefit remain unknown. Invasive and noninvasive techniques exist for assessing therapeutic efficacy, but determination of which is more appropriate awaits a wider experience and more direct comparison.     

Benefits of treatment with implantable cardioverter-defibrillators in patients with stable ventricular tachycardia without cardiac arrest.

BACKGROUND--The availability of implantable cardioverter-defibrillators (ICD) that are capable of antitachycardia pacing may lead to an increased use of ICDs in patients with haemodynamically tolerated ventricular tachycardia without a history of cardiac arrest. The frequency of potentially life-threatening fast ventricular tachycardias (cycle length < 250 ms) was investigated in patients who had a third generation ICD with endocardial leads implanted because they had haemodynamically tolerated ventricular tachycardia without a history of cardiac arrest. METHODS--Between January 1990 and October 1993, 50 patients (age (mean (SD)) 60 (11); ejection fraction 39 (16)%; 82% with coronary artery disease and 8% with dilated cardiomyopathy) with haemodynamically tolerated ventricular tachycardia (cycle length (mean (SD)) 348 (60) ms; range 250-500 ms) and without a history of cardiac arrest were treated with third generation ICDs that were capable of antitachycardia pacing. Fast ventricular tachycardia had been induced in 14 (28%) during baseline electrophysiological study. The benefit of ICD treatment was estimated as the difference between total mortality and the occurrence of fast ventricular tachycardia that would have been fatal if it had not been terminated. RESULTS--During follow up of 17 (12) months, 33 patients (66%) had a total of 3861 episodes of ventricular tachycardia. 91% of these episodes were terminated by antitachycardia pacing. 11 patients (22%) had episodes of potentially life-threatening fast ventricular tachycardia and 3 of these also had inducible fast ventricular tachycardia. One patient died suddenly 27 months after implantation. The difference between survival without fast ventricular tachycardia and total mortality was 9%, 12%, 27%, and 27% at 6, 12, 18, and 24 months, respectively. CONCLUSIONS--About a fifth of patients who had been given an ICD to treat haemodynamically tolerated ventricular tachycardia and who had no history of cardiac arrest experienced fast ventricular tachycardia during follow up requiring immediate cardioversion. Prospective studies are needed to investigate whether the prognosis of patients with a history of haemodynamically tolerated ventricular tachycardia without cardiac arrest is improved by ICD therapy.     

Diverse mechanisms of unexpected cardiac arrest in advanced heart failure

To define the mechanisms of unexpected cardiac arrest in advanced heart failure, we reviewed the causes of cardiac arrest as established from electrocardiographic monitoring and from clinical and autopsy data in patients hospitalized for cardiac transplantation evaluation and management of advanced heart failure (mean left ventricular ejection fraction, 0.18 +/- 0.08) who were stable while on vasodilator and diuretic therapy such that hospital discharge to home was anticipated. Twenty-one cardiac arrests occurred in 20 of 216 (9%) such patients during a 4-year period. Heart failure was due to coronary artery disease with prior myocardial infarction in 13 patients and nonischemic cardiomyopathy in seven patients. The rhythm at the time of arrest was severe bradycardia or electromechanical dissociation (BA/EMD) in 13 (62%) patients. The precipitating cause of the BA/EMD arrest was coronary artery thrombosis or embolism in two patients, pulmonary embolism in one patient, hyperkalemia in two patients, and unexplained hypoglycemia in one patient. In seven of 13 (54%) patients, a precipitating cause of the bradycardia arrest could not be established. Only eight of 21 (38%) arrests were due to ventricular tachycardia or fibrillation (VT/VF), and all occurred in patients with prior myocardial infarction (p = 0.02 vs. BA/EMD arrests). Two VT/VF arrests were due to acute or recent infarction, and one patient had hyperkalemia. The patients who suffered a BA/EMD arrest were similar to those who had a VT/VF arrest in age, ventricular arrhythmia history, ventricular function, and serum potassium levels. Serum sodium levels were lower in patients with BA/EMD arrests (129 +/- 3 vs. 133 +/- 4 meq/l, p = 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)     

大剂量胺碘酮对持续性室性心动过速的纠治

目的 :观察大剂量胺碘酮治疗持续性室性心动过速 ( SVT)的临床疗效及副作用。方法 :初始以胺碘酮 15 0 m g静脉注射 (静注 ) ,5～ 10 min注射完毕 ,必要时重复 1～ 2个初始量 ,继以 0 .5～ 5 m g/ min静脉维持 3～ 8d。结果 :6例 SVT均在静脉用药 2 h内得到控制 ,2 h内静脉胺碘酮用量 3 90～ 5 4 0 ( 4 68.4± 5 4 .7) m g;2 4 h内静脉平均用量 10 0 0～ 180 0 ( 14 10 .3± 3 5 6.5 ) m g,除注射局部均发生不同程度的静脉炎外 ,未见低血压、心功能恶化及致心律失常作用。结论 :短期内经静脉大剂量应用胺碘酮安全有效     

Right ventricular longitudinal strain correlates well with right ventricular stroke work index in patients with advanced heart failure referred for heart transplantation

BackgroundRight ventricular (RV) systolic function has a critical role in determining the clinical outcome and success of using left ventricular assist devices (LVADs) in patients with refractory heart failure. Tissue Doppler and M-mode measurements of tricuspid systolic motion (tricuspid S′ and tricuspid annular plane systolic excursion [TAPSE]) are the most currently used methods for the quantification of RV longitudinal function; RV deformation analysis by speckle-tracking echocardiography (STE) has recently allowed the analysis of global RV longitudinal function. Using cardiac catheterization as the reference standard, this study aimed at exploring the correlation between RV longitudinal function by STE and RV stroke work index (RVSWI) in patients referred for cardiac transplantation.Methods and ResultsRight-side heart catheterization and transthoracic echo Doppler were simultaneously performed in 41 patients referred for cardiac transplantation evaluation for advanced systolic heart failure. Thermodilution RV stroke volume and invasive pulmonary pressures were used to obtain RVSWI. RV longitudinal strain (RVLS) by STE was assessed averaging all segments in apical 4-chamber view (global RVLS) and by averaging RV free-wall segments (free-wall RVLS). Tricuspid S′ and TAPSE were also calculated. No significant correlations were found for TAPSE or tricuspid S′ with RVSWI (r = 0.14; r = 0.06; respectively). Close negative correlations between global RVLS and free-wall RVLS with the RVSWI were found (r = ?0.75; r = ?0.82; respectively; both P < .0001). Furthermore, free-wall RVLS demonstrated the highest diagnostic accuracy (area under the receiver operating characteristic (ROC) curve 0.90) and good sensitivity and specificity of 92% and 86%, respectively, to predict depressed RVSWI using a cutoff value of less than ?11.8%.ConclusionsIn a group of patients referred for heart transplantation, TAPSE and tricuspid S′ did not correlate with invasively obtained RVSWI. RV longitudinal deformation analysis by STE correlated well with RVSWI, providing a better estimation of RV systolic performance.     

充血性心力衰竭患者非持续性室性心动过速与心脏性死亡的关系

目的探讨充血性心力衰竭(CHF)患者非持续性室性心动过速(NSVT)与心脏性死亡之间的关系。方法对52例CHF伴NSVT患者,根据住院期间是否发生心脏性死亡,分为死亡组(13例),存活组(39例),分析两组心电图及临床特征。结果死亡组NSVT的发作阵数高,频率快,每阵持续搏动数多,QRS波时限宽,多形性VT发生率高(P<0．05～0．001);常规心电图中,死亡组室内传导阻滞发生率高,QT和QTc间期长(P<0．05～0．005);两组间心功能级别无差异(P>0．05),但死亡组左室射血分数明显低于存活组(P<0．001)。结论CHF患者伴NSVT,并具有上述特征时,有发生心脏性死亡的高度危险。     

Propafenone therapy for ventricular tachycardia in the setting of congestive heart failure

The combined occurrence of impaired left ventricular function and ventricular tachyarrhythmias portend a high annual mortality. Although antiarrhythmic drugs can reduce ventricular arrhythmias, the prognosis may be unchanged. We administered propafenone to 12 patients with ventricular tachyarrhythmias and left ventricular ejection fractions less than 40%. Propafenone significantly reduced isolated ventricular premature depolarizations, couplets, and ventricular tachycardia on ambulatory monitoring. Propafenone eliminated all exercise provocable ventricular tachycardia. Propafenone additionally abolished ventricular tachycardia inducible by programmed stimulation in five of six patients. In eight patients studied before and during therapy, there was no significant change in left ventricular ejection fraction determined by nuclear ventriculography. Propafenone was discontinued in three patients due to side effects. All patients remain alive and without recurrence of clinically significant arrhythmia over a mean follow-up period of 14 months. Propafenone is an effective drug for the management of ventricular tachyarrhythmias, and may be used in patients with impaired left ventricular function.     

Characterization of sustained atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure

INTRODUCTION: Atrial arrhythmias often complicate congestive heart failure (CHF). We characterized inducible atrial tachyarrhythmias and electrophysiologic alterations in dogs with CHF and atrial enlargement produced by rapid ventricular pacing. METHODS AND RESULTS: Endocardial pacing leads were implanted in the right ventricle, right atrium, and coronary sinus in 18 dogs. The right ventricular lead was connected to an implanted pacemaker capable of rapid ventricular pacing. The atrial leads were used to perform electrophysiologic studies in conscious animals at baseline in all dogs, during CHF induced by rapid ventricular pacing at 235 beats/min in 15 dogs, and during recovery from CHF in 6 dogs. After 20 +/- 7 days of rapid ventricular pacing, inducibility of sustained atrial tachycardia (cycle length 120 +/- 12 msec) was enhanced in dogs with CHF. Atrial tachycardia required a critical decrease in atrial burst pacing cycle length (< or = 130 msec) for induction and often could be terminated by overdrive pacing. Calcium antagonists (verapamil, flunarizine, ryanodine) terminated atrial tachycardia and suppressed inducibility. Effective refractory periods at 400- and 300-msec cycle lengths in the right atrium and coronary sinus were prolonged in dogs with CHF. Atrial cells from dogs with CHF had prolonged action potential durations and reduced resting potentials and delayed afterdepolarizations (DADs). Mitochondria from atrial tissue from dogs with CHF were enlarged and had internal cristae disorganization. CONCLUSIONS: CHF promotes inducibility of sustained atrial tachycardia. Based on the mode of tachycardia induction, responses to pacing and calcium antagonists, and presence of DADs, atrial tachycardia in this CHF model has a mechanism most consistent with DAD-induced triggered activity resulting from intracellular calcium overload.     

Prospective evaluation of a protocol for induction of sustained ventricular tachycardia in patients referred to a tertiary centre.

All eight stages of a stimulation protocol that used one then two extrastimuli from the right ventricular apex in sinus rhythm and three ventricular drive rates (100, 120, and 140 beats/min) were performed in 24 patients with recurrent spontaneous sustained ventricular tachycardia despite drug treatment. Twenty two of the patients had sustained a previous myocardial infarct and 18 were on long term treatment with amiodarone. Sustained (greater than 30 s) ventricular tachycardia was induced in all patients. Two extrastimuli were significantly more likely to induce sustained ventricular tachycardia than one extrastimulus, both overall and individually for the three ventricular drive rates. A ventricular drive rate of 140 beats/min was significantly more likely to induce ventricular tachycardia than ventricular drive rates of 100 and 120 beats/min which were significantly more effective than sinus rhythm. A ventricular drive rate of 140 beats/min with one or two extrastimuli induced ventricular tachycardia in 23/24 (95%) of the patients in this study. The full eight stage protocol was progressive separately for both extrastimuli and ventricular drive rate but the last two stages (ventricular drive rate of 140 beats/min with one or two extrastimuli) were as effective as the entire protocol in inducing ventricular tachycardia.     

Propafenone-mexiletine combination for the treatment of sustained ventricular tachycardia.

OBJECTIVES. The purpose of this study was to explore the efficacy of combined therapy with propafenone and mexiletine for control of sustained ventricular tachycardia. BACKGROUND. Combination antiarrhythmic drug therapy may enhance efficacy and lead to control of ventricular arrhythmias in some patients. Few reports have studied the combination of class IB and class IC drugs. Thus, this study was designed to investigate a combination of mexiletine and propafenone in patients with refractory ventricular tachycardia. METHODS. Sixteen patients with sustained ventricular tachycardia had their clinical arrhythmia induced by programmed stimulation. Procainamide and propafenone alone failed to prevent reinduction of tachycardia in all. Mexiletine was subsequently added to propafenone and programmed stimulation was repeated. RESULTS. With combination therapy ventricular tachycardia was noninducible in three patients (19%). A fourth who had presented with polymorphic ventricular tachycardia had slow bundle branch reentry (cycle length 500 ms) induced. In the other 12, tachycardia cycle length increased from 262 +/- 60 ms at baseline to 350 +/- 82 ms with propafenone and to 390 +/- 80 ms with propafenone plus mexiletine (p less than 0.0001 compared with baseline). Hemodynamic deterioration requiring defibrillation occurred in six patients at baseline study, in five taking propafenone and in two taking both drugs. CONCLUSIONS. The combination of propafenone and mexiletine is effective in suppressing the induction of ventricular tachycardia in some patients refractory to procainamide and propafenone alone. In those in whom ventricular tachycardia could still be induced, the rate was slower and hemodynamically tolerated.     

Optimizing cardiac resynchronization therapy in advanced heart failure

Up to 30% of cardiac resynchronization therapy (CRT) patients are considered to be "nonresponders." While the absolute number might increase because of the increased use of CRT, this proportion remains stable. As a result, there is a pressing need for guidelines for practicing clinicians to maximize the effectiveness of CRT. This clinician update describes easy-to-comprehend cases that might provide a practical insight for cardiologists, as well as for all professionals who take care of patients with heart failure who have undergone CRT.